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At least 451 records · Page 25Linked to original sources
PubMed2006

Early changes of small intestine function in rats after liver transplantation.

OBJECTIVE: The aims of this study were to explore the concomitant changes of the barrier function, bacterial translocation, absorption, and small intestinal motility in rats after liver transplantation and to correlate these changes with levels of plasma endotoxin. METHODS: Thirty Wistar rats were divided randomly between a sham operation group (n=10) and a liver transplantation group (n=10 pairs). The intestinal transit function, intestinal permeability, bacterial translocation, absorption function, levels of plasma endotoxin, and nitrogen monoxide (NO) changes in plasma and small intestinal mucosa were monitored in the two groups. The expression of iNOS mRNA in the intestine was investigated by reverse transcriptase-polymerase chain reactions. RESULTS: Significant differences were observed between the liver transplantation group and the sham operation group for aspects of intestinal transit function, intestinal permeability, bacterial translocation, absorption function, and NO changes in both plasma and small intestine. Compared with the sham operation group, the expression of iNOS mRNA was significantly increased (P<.05) in the small intestine of rats that had undergone liver transplantation. CONCLUSION: The functions of motility, barrier, and absorption in the intestine were decreased among rats that had undergone liver transplantation. Reduced motility in the small intestine of the rats following liver transplantation may be related to the enhanced expression of iNOS in the intestine with a negative correlation to plasma levels of endotoxin.

Animals↗
PubMed2002

Liver response to indomethacin-induced intestinal injury.

The aim of our study was to evaluate the impact of impaired barrier function of the small intestine induced by indomethacin on biochemical markers of liver damage (serum levels of alanine aminotransferase, aspartate aminotransferase, bilirubin), and liver functional parameters (serum concentration of albumin, liver DNA synthesis). Indomethacin (Sigma) was administered in 2 injections in a dose of 7.5 mg/kg subcutaneously spaced 24 hours apart, rats were sacrificed 24, 48 or 72 hours after the second dose of indomethacin. Control rats received indomethacin vehicle (5% NaHCO3, pH 7.4, 1.0 ml/kg) in the same manner. Small intestine injury was approved by increased permeability (measured as a lactulose-mannitol index). Significant increase of small intestine DNA synthesis (estimated by incorporation of 3H thymidine) in indomethacin-treated rats 48 (p < 0.01) and 72 (p < 0.05) hours after the second dose of indomethacin documents induction of reparative process. All biochemical markers of liver injury were significantly decreased in indomethacin treated rats in all recorded intervals (p < 0.05). By contraries, serum concentration of albumin, which predicates about liver function, was in indomethacin-treated rats significantly decreased in all intervals (p < 0.01). To explain these contrarious results of indomethacin-induced impaired barrier function of the small intestine on the liver deserves further studies.

Animals↗
PubMed2000

Inhibitory effects of intestinal mucus on bacterial adherence to cultured intestinal epithelial cells after surface burns.

OBJECTIVE: To investigate the relationship between intestinal mucus IgA content and mucus barrier function after surface burns. METHODS: Detection of IgA content in mucus was performed by enzyme linked immunosorbent assay (ELISA) at different time points after burns. Bacterial adherence to cultured epithelial cells (IEC-6) in vitro using E. coli was assessed for each group. RESULTS: The intestinal mucus barrier function declined, parallel to a decrease in IgA content after surface burn in mice. In the normal control group, mucus IgA content was 2.32 D lambda, and 2.51, 1.76, 1.49, 1.06 D lambda at 0.5 h, 1 h, 6 h and 24 h after burn, respectively. Bacterial adherence rate was 0.53 in control group, and 0.46, 0.69, 0.58, 0.81 at 0.5 h, 1 h, 6 h, 24 h after burn, respectively. CONCLUSION: The decrease of intestinal mucus IgA contents is one of the reasons why intestinal mucus barrier function declines after burns.

Animals↗
PubMed2007

Interleukin-6 induces keratin expression in intestinal epithelial cells: potential role of keratin-8 in interleukin-6-induced barrier function alterations.

Keratin 8 (K8) and keratin-18 (K18) are the major intermediate filament proteins in the intestinal epithelia. The regulation and function of keratin in the intestinal epithelia is largely unknown. In this study we addressed the role and regulation of K8 and K18 expression by interleukin 6 (IL-6). Caco2-BBE cell line and IL-6 null mice were used to study the effect of IL-6 on keratin expression. Keratin expression was studied by Northern blot, Western blot, and confocal microscopy. Paracellular permeability was assessed by apical-to-basal transport of a fluorescein isothiocyanate dextran probe (FD-4). K8 was silenced using the small interfering RNA approach. IL-6 significantly up-regulated mRNA and protein levels of K8 and K18. Confocal microscopy showed a reticular pattern of intracellular keratin localized to the subapical region after IL-6 treatment. IL-6 also induced serine phosphorylation of K8. IL-6 decreased paracellular flux of FD-4 compared with vehicle-treated monolayers. K8 silencing abolished the decrease in paracellular permeability induced by IL-6. Administration of dextran sodium sulfate (DSS) significantly increased intestinal permeability in IL-6-/- mice compared with wild type mice given DSS. Collectively, our data demonstrate that IL-6 regulates the colonic expression of K8 and K18, and K8/K18 mediates barrier protection by IL-6 under conditions where intestinal barrier is compromised. Thus, our data uncover a novel function of these abundant cytoskeletal proteins, which may have implications in intestinal disorders such as inflammatory bowel disease wherein barrier dysfunction underlies the inflammatory response.

Animals↗
PubMed2001

Effect of surgical manipulation of the rat intestine on enterocyte populations.

BACKGROUND: The intestine is susceptible to operations at remote locations, and the barrier function is altered during intestinal manipulation, leading to bacterial or endotoxin translocation into the systemic circulation. One of the mainstays for the maintenance of the integrity of the barrier function is epithelial cell proliferation and migration. The present study looked at the effect of gut manipulation after laparotomy on different cell populations of the intestinal epithelium. METHODS: Surgical manipulation of the gut was performed by opening the abdominal wall and handling the intestine, as is done during laparotomy. Villus and crypt cells were isolated at different time periods after gut manipulation, and mitochondria were prepared from isolated enterocytes. The effects of surgical manipulation on enterocytes and isolated mitochondria were studied. RESULTS: Mechanical manipulation of the gut resulted in alterations in the intestinal epithelium, as shown by decreased cell viability and yield in the crypt cells. The alterations were associated with actin reorganization, as well as with altered cell proliferation and adenosine deaminase activity. At the mitochondrial level, altered mitochondrial function, such as decreased respiratory control ratio, increased 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide reduction, and induction of permeability transition in the crypt cells, was observed. These alterations were maximal 1 hour after surgical manipulation and partially recovered to normal by 24 hours. CONCLUSIONS: Mechanical manipulation of the gut that occurs during any abdominal operation induces alterations in the intestine, both at the cellular and the subcellular levels. The crypt cells bear the brunt of the damage, and the reversibility of the damage is possibly brought about by increased proliferation and movement of the cells.

Actins↗
PubMed2000

Mechanism of extracellular calcium regulation of intestinal epithelial tight junction permeability: role of cytoskeletal involvement.

Recent studies suggest that an abnormal increase in intestinal tight junction (TJ) permeability may be an important etiologic factor in number of diseases including Crohn's disease, NSAID-associated enteritis, and various infectious diarrheal syndromes. The intracellular processes involved in regulation of intestinal epithelial TJ permeability, however, remain poorly understood. In this study, we used cultured Caco-2 intestinal epithelial cells to examine the intracellular processes involved in extracellular Ca(++) modulation of intestinal epithelial monolayer TJ barrier. Incubation of the filter-grown Caco-2 intestinal monolayers in Ca(++)-free solution (CFS), consisting of modified Krebs-buffer solution containing 0 mM Ca(++) and 1 mM EGTA, resulted in a rapid drop in Caco-2 epithelial resistance and increase in epithelial permeability to paracellular markers mannitol and inulin, indicating an increase in TJ permeability. The increase in Caco-2 TJ permeability was rapidly reversed by the re-introduction of Ca(++) (1.8 mM) into the incubation medium. The CFS-induced increase in Caco-2 TJ permeability was associated with separation of the cytoplasmic and transmembrane TJ proteins, ZO-1 and occludin, and formation of large intercellular openings between the adjoining cells. The CFS-induced modulation of TJ barrier was associated with activation of myosin light chain kinase (MLCK) activity and centripetal retraction of peri-junctional actin and myosin filaments. The inhibition of CFS-induced activation of Caco-2 MLCK with MLCK inhibitor (ML-7) prevented the CFS-induced retraction of actin and myosin filaments and the subsequent alteration of TJ barrier function and structure. Our results suggested that the CFS-induced alteration of TJ proteins and functional increase in TJ permeability was mediated by Caco-2 MLCK activation and the resultant contraction of the peri-junctionally located actin-myosin filaments. Consistent with the role of MLCK in this process, selected inhibitors of Mg(++)-myosin ATPase and metabolic energy, but not protein synthesis inhibitors, also prevented the CFS-induced retraction of actin and myosin filaments and the subsequent increase in TJ permeability. In conclusion, our results indicate that extracellular Ca(++) is crucial for the maintenance of intestinal epithelial TJ barrier function. The removal of extracellular Ca(++) from the incubation medium causes activation of Caco-2 MLCK, which in turn leads to an increase in intestinal monolayer TJ permeability.

Actins↗
PubMed2006

Intestinal permeability and systemic endotoxemia after laparotomic or laparoscopic cholecystectomy.

OBJECTIVE: Because laparoscopic cholecystectomy (LC) is widely recognized as a "mild" or "mini-invasive" kind of surgery, in this prospective nonrandomized study, we investigated the effect of intestinal manipulation on intestinal permeability and endotoxemia, in patients undergoing elective cholecystectomy by comparing the laparoscopic with the laparotomic approach. SUMMARY BACKGROUND DATA: The intestine is susceptible to operations at remote locations, and the barrier function is altered during intestinal manipulation, leading to bacterial or endotoxin translocation into the systemic circulation. METHODS: Forty-three patients undergoing elective cholecystectomy were divided into either the laparotomic (n = 22) or laparoscopic (n = 21) approach. Intestinal permeability was measured preoperatively and at day 1 and day 3 after surgery using the lactulose/mannitol absorption test. Serial venous blood samples were taken at 0, 30, 60, 90, 120, and 180 minutes, and at 12, 24, and 48 hours after surgery, for endotoxin measurement using the chromogenic limulus amoebocyte lysate assay. RESULTS: Intestinal permeability was significantly increased at day 1 [0.106 +/- 0.005 (mean +/- SEM)] in the laparotomic group compared with the preoperative level (0.019 +/- 0.005, P < 0.05) and to the laparoscopic group at day 1 (0.019 +/- 0.005, P < 0.05), which showed no change in comparison with the preoperative level. A significantly higher concentration of systemic endotoxin was detected intraoperatively in the laparotomic group of patients in comparison to the laparoscopic group (P < 0.05). There was a significant positive correlation between systemic endotoxemia and intestinal permeability (r(s) = 0.958; P = 0.001). CONCLUSIONS: An increase in intestinal permeability and a greater degree of systemic endotoxemia are observed during laparotomic cholecystectomy. This suggests that intestinal manipulation may impair gut mucosal barrier function and contribute to the systemic inflammatory response see in open cholecystectomy.

Adult↗
PubMedDate not supplied

[Intestinal and systemic endotoxaemia after laparotomic or laparoscopic cholecystectomy].

Since laparoscopic cholecystectomy (LC) is widely recognised as being a "mild" or minimally invasive kind surgery, the aim of this prospective non-randomised study was to investigate the effect of intestinal manipulation on intestinal permeability and endotoxaemia in patients undergoing elective cholecystectomy, comparing the laparoscopic and laparotomic approaches. The intestine is susceptible to operations at remote locations, and the barrier function is altered during intestinal manipulation, leading to bacterial or endotoxin translocation into the systemic circulation. Fifty-three patients undergoing elective cholecystectomy were divided into two groups on the basis of laparotomic (n = 27) or laparoscopic (n = 26) approach. Intestinal permeability was measured preoperatively, and on day 1 and day 3 after surgery using the lactulose/mannitol absorption test. Serial venous samples were taken at 0, 30, 60, 90, 120 and 180 minutes, and at 12, 24 and 48 hours after surgery, for endotoxin measurement using the chromogenic limulus amoebocyte lysate assay. Intestinal permeability was significantly increased on day 1 [0.106 +/- 0.0005 (mean +/- S.E.M.)] in the laparotomic group compared to the preoperative level (0.019 +/- 0.005, p < 0.05) and to the laparoscopic group on day 1 (0.019 +/- 0.005, p < 0.05) which showed no change in comparison with the preoperative level. A significantly higher concentration of systemic endotoxin was detected intraoperatively in the laparotomic group of patients in comparison with the laparoscopic group (p < 0.05). There was significant positive correlation between systemic endotoxaemia and intestinal permeability (rs = 0.958; p = 0.001). An increase in intestinal permeability and degree of systemic endotoxaemia are observed during laparotomic cholecystectomy. This suggets that intestinal manipulation may impair the mucosal barrier function of the gut and contribute to the systemic inflammatory response seen in open cholecystectomy.

Adult↗
PubMed2002

Role of transporters in the tissue-selective distribution and elimination of drugs: transporters in the liver, small intestine, brain and kidney.

Cumulative studies have revealed the importance of transporters in drug disposition in the body. Recently, organic anion transporters such as organic anion transporting polypeptides (OATPs), organic anion transporters (OATs) and multidrug resistance associated proteins (MRPs) have been identified. Their broad substrate specificity as well as the multiplicity of transporter gene products make these transporters suitable detoxification systems in the body. OATPs and OATs are responsible for the hepatic and renal uptake of organic anions, respectively, while MRP2 is a major transporter involved in the biliary excretion of organic anions. OATPs and MRP2 are involved in the hepatobiliary transport of pravastatin and temocaprilat. These are good examples of hepatobiliary transport maximizing their pharmacological effects, but minimizing their side-effects. Taking into consideration tissue-selective expression and substrate specificity, transporters are useful for delivering small molecules to target tissues. MRPs are also suggested to be involved in the barrier function in the small intestine, blood-brain barrier and blood-cerebrospinal fluid barriers by extruding their ligands into the luminal side. In this manuscript, we have summarized recent studies by others and ourselves on the role of these transporters in the tissue selective distribution and elimination of drugs.

Animals↗
PubMed2005

[Study on the mechanism by which Rhubarb protects the mucosal barrier of intestine of mouse].

OBJECTIVE: To observe the influence of Rhubarb on the the excretion of Type II PLA2 and lysozyme of small intestine of mouse. METHODS: Forty ICR mice were randomized to two groups. In the experiment group, the mice were gavaged with 0.3 ml 10% Rhubarb decoction every 8 hours; in the control group, the mice were given normal saline instead of Rhubarb decoction. After 24 hours, the mice were subjected to cervical dislocation, and their jejunum and ileum were taken out. The lumen of each resected intestine was rinsed with 100 g/L acetic acid, and the washed intestines from each mouse were cut into pieces 1-2 mm in length. Then the perfusate and homogenate were prepared, lyophilized, sealed, and stored at -20 degrees C. The Type II PLA2 activity and lysozyme were assayed respectively. RESULTS: The Type II PLA2 activities and lysozyme of homogenate in Rhubarb group were lower than those in Saline group (P<0.01). The type II PLA2 activities and lysozyme of perfusate in Rhubarb group were higher than those in Saline group (P<0.01). CONCLUSION: Rhubarb can stimulate the small intestine of mice to excrete Type II PLA2 and lysozyme, thus resulting in the increase of Type II PLA2 and lysozyme contents in the intestinal tract and enhancing the function of mucosal barrier of intestine.

Animals↗
PubMed2003

Proinflammatory cytokines disrupt epithelial barrier function by apoptosis-independent mechanisms.

It is well known that inflammatory conditions of the intestinal mucosa result in compromised barrier function. Inflammation is characterized by an influx into the mucosa of immune cells that influence epithelial function by releasing proinflammatory cytokines such as IFN-gamma and TNF-alpha. Mucosal barrier function is regulated by the epithelial apical junctional complex (AJC) consisting of the tight junction and the adherens junction. Since the AJC regulates barrier function, we analyzed the influence of IFN-gamma and TNF-alpha on its structure/function and determined the contribution of apoptosis to this process using a model intestinal epithelial cell line, T84, and IFN-gamma and TNF-alpha. AJC structure/function was analyzed by confocal microscopy, biochemical analysis, and physiologic measurement of epithelial gate/fence function. Apoptosis was monitored by determining cytokeratin 18 cleavage and caspase-3 activation. IFN-gamma induced time-dependent disruptions in epithelial gate function that were potentiated by coincubation with TNF-alpha. Tight junction fence function was somewhat disrupted. Cytokine treatment was associated with internalization of AJC transmembrane proteins, junction adhesion molecule 1, occludin, and claudin-1/4 with minimal effects on the cytoplasmic plaque protein zonula occludens 1. Detergent solubility profiles of junction adhesion molecule 1 and E-cadherin and their affiliation with "raft-like" membrane microdomains were modified by these cytokines. Inhibition of cytokine-induced apoptosis did not block induced permeability defects; further emphasizing their primary influence on the epithelial AJC structure and barrier function. Our findings for the first time clearly separate the proapoptotic effects of IFN-gamma and TNF-alpha from their abilities to disrupt barrier function.

Adherens Junctions↗
PubMed2000

Modulation of barrier function during Fas-mediated apoptosis in human intestinal epithelial cells.

BACKGROUND & AIMS: Intestinal epithelial cell apoptosis occurs continually without apparent permeability defects and is increased in response to intestinal inflammation. We hypothesized that increased, immune-mediated apoptosis during inflammation might result in barrier dysfunction of the epithelium. METHODS: T84 cells were cultured as a polarized monolayer and exposed to agonist antibody to Fas. Barrier function was assessed by transepithelial resistance and permeability measurements. Immunofluorescent staining was used to examine junctional protein expression. RESULTS: Fas expression is predominantly basolateral in polarized T84 monolayers. Basolateral cross-linking of the Fas receptor resulted in T84 cell apoptosis and a loss of 50% of the cells within 24 hours. Apoptosis was coincident with a decrease in transepithelial electrical resistance and increased flux of small but not large molecules. Preservation of barrier function was associated with dramatic rearrangement of tight junctions and desmosomal junctions in apoptotic monolayers. E-cadherin-mediated cell contact was maintained between intact cells in the monolayer, thus sealing gaps created by apoptotic cells. Apoptosis and barrier dysfunction could be prevented by caspase inhibition. CONCLUSIONS: Immune-mediated apoptosis of intestinal epithelial cells may contribute to the permeability defects associated with inflammatory conditions of the bowel, but the intestinal epithelium is remarkably resilient in the face of apoptosis.

Antibodies↗
PubMed2002

Gut barrier permeability, reticuloendothelial system function and protease inhibitor levels following intestinal ischaemia and reperfusion--effects of pretreatment with N-acetyl-L-cysteine and indomethacin.

BACKGROUND: Pathophysiological mechanisms and ways to intervene on intestinal barrier dysfunction following small intestinal ischaemia and prolonged reperfusion are still not fully clarified. AIMS: To evaluate the effect of oxygen free radical and prostaglandin inhibition on intestinal barrier injury following intestinal ischaemia/reperfusion. METHODS: Endothelial and epithelial barrier permeability was evaluated by clearance of radiolabelled albumin. Parameters included 125I-Escherichia coli uptake rate index, host reticuloendothelial system function and organ distribution, as well as protease inhibitor and proenzyme activities in rats subjected to small intestinal ischaemia for 40 minutes followed by 12 hours reperfusion (ischaemia/reperfusion), pretreated with N-acetyl-L-cysteine or indomethacin. RESULTS: Following ischaemia/reperfusion, endothelial and epithelial permeability increased, reticuloendothelial system activation occurred and plasma protease inhibitors were consumed. N-acetyl-L-cysteine pretreatment resulted in improved endothelial and epithelial barrier integrity, a decrease in protease inhibitor consumption and less pronounced reticuloendothelial system activation. Pretreatment with indomethacin was not effective. CONCLUSION: Oxygen free radicals seem to play an important role in the development of intestinal barrier impairment following ischaemia/reperfusion. N-acetyl-L-cystine may be a potential agent for preventing ischaemia/reperfusion damage.

Acetylcysteine↗
PubMed2006

Stress signaling pathways activated by weaning mediate intestinal dysfunction in the pig.

Weaning in the piglet is a stressful event associated with gastrointestinal disorders and increased disease susceptibility. Although stress is thought to play a role in postweaning intestinal disease, the mechanisms by which stress influences intestinal pathophysiology in the weaned pig are not understood. The objectives of these experiments were to investigate the impact of weaning on gastrointestinal health in the pig and to assess the role of stress signaling pathways in this response. Nineteen-day-old pigs were weaned, and mucosal barrier function and ion transport were assessed in jejunal and colonic tissues mounted on Ussing chambers. Weaning caused marked disturbances in intestinal barrier function, as demonstrated by significant (P < 0.01) reductions in transepithelial electrical resistance and increases in intestinal permeability to [3H]mannitol in both the jejunum and colon compared with intestinal tissues from age-matched, unweaned control pigs. Weaned intestinal tissues exhibited increased intestinal secretory activity, as demonstrated by elevated short-circuit current that was sensitive to treatment with tetrodotoxin and indomethacin, suggesting activation of enteric neural and prostaglandin synthesis pathways in weaned intestinal tissues. Western blot analyses of mucosal homogenates showed increased expression of corticotrophin-releasing factor (CRF) receptor 1 in the jejunum and colon of weaned intestinal tissues. Pretreatment of pigs with the CRF receptor antagonist alpha-helical CRF(9-41), which was injected intraperitoneally 30 min prior to weaning, abolished the stress-induced mucosal changes. Our results indicate that weaning stress induces mucosal dysfunction mediated by intestinal CRF receptors and activated by enteric nerves and prostanoid pathways.

Animals↗
PubMed1989

Characterization of mitomycin C-induced gastrointestinal damage. II. In vitro everted sac experiment.

The everted gut sac technique was employed to clarify the effects of preadministration of mitomycin C (MMC) on intestinal transport of various drugs. Loss of intestinal tissue weight and increase in mucosal-to-serosal fluxes of passively absorbed drugs were noted in the case of MMC pretreatment, although the extent of the latter effect varied according to the inherent absorbability of each drug. The maximal effect of MMC on intestinal tissue weight and transport of sulfanilamide, a model of a passively absorbed drug, was observed 48 hr after pretreatment. The increase in the transfer of sulfanilamide correlated well with the MMC-induced decrease in intestinal tissue weight. These phenomena may result from the shortened transfer distance from mucosal to serosal fluid and impaired barrier function of the intestinal mucosa. On the other hand, transport of actively absorbed 3-O-methyl-D-glucose was not influenced by MMC pretreatment, which could be explained by an increment in the passive permeation counterbalancing the decrement in the active permeation. The present study also suggested that the measurement of transport of drugs through everted gut sacs might be useful as a simple and qualitative index of gastrointestinal mucosal damage.

3-O-Methylglucose↗
PubMed1990

[Disorders of zinc transport through the ileal epithelium in vitamin A deficiency and ischemia].

By means of histochemical revealing of zinc and applying radioactive isotope 65Zn accumulation, absorption and distribution of cations of this metal in the mucous membrane of the iliac intestine have been studied in chicken, normal, at ischemia and at A-avitaminosis. An essential zinc-depositing ability is peculiar to coverings of mucus upon the intestine epithelium, and among intracellular components--to smooth endoplasmic reticulum. A-avitaminosis and especially ischemia result in increasing permeability of the apical part of the external membrane of epitheliocytes, in overloading of the latter with zinc cations, when they are introduced into the intestine, as well as in decreasing transepithelial transport of zinc. The changes mentioned are accompanied with certain disturbances in the barrier function of the intestinal epithelium.

Animals↗
PubMed1998

Correlation between electrophysiological phenomena and transport of macromolecules in intestinal epithelium.

This review discuss some recent findings in the study of the regulation of the permeability of the intestinal epithelial layer. Comparison of electrical phenomena and transport of macromolecules suggests that secretory activity and increased transepithelial transport of macromolecules are related when secretion is mediated by the Ca2+ and PKC dependent pathways. The transport of the macromolecules is via the transcellular and via the paracellular route. The barrier function of the intestinal epithelium may be diminished during nervous (acetylcholine)- and immuno-(histamine) mediated secretion. It is hypothesised that some bacterial toxins may also induce Ca2+ and PKC dependent secretion and thereby can reduce the epithelial barrier. The cAMP and cGMP mediated secretion, which can be recognised by their long-lasting transepithelial potential changes, are not coupled to increased transepithelial transport of macromolecules. Some forms of secretory diarrhea may therefore be related to the development of food-allergy or inflammation.

Biological Transport, Active↗